Background Diltiazem stands out as one of the front-line drugs administered in the emergency department to achieve acute rate control in patients suffering from atrial fibrillation with rapid Ventricular Response. One of the cytochrome enzymes involved in the metabolism of diltiazem is cytochrome P450 2D6 (CYP2D6). Interindividual differences can act on drug metabolism and thus drug efficacy due to the genetic polymorphism induced by the CYP2D6 enzyme. This study explores the association between the efficacy of diltiazem and the genetic polymorphism of CYP2D6 in patients with atrial fibrillation with rapid ventricular response. Results 87 out of 93 individuals with ventricular rate > 120 beats/min constituted the patient cohort. The patients were administered 0.25 mg/kg diltiazem intravenously. As a second dose, 0.35 mg/kg diltiazem was administered to patients who reportedly did not receive adequate drug efficacy. Heart rate control was considered to be achieved in patients whose heart rate fell below 110 beats/min and did not rise above 110 beats/min for 2 h. CYP2D6 *2, *3, *4 and *10 represent allele variants and *1 represents wild type (wt) allele. Achieving rate control after one or two doses of diltiazem in normal allele (wt/wt) carriers proved significantly higher than wt/*2, wt/*4 and wt/*10 heterozygous variant carriers. No significant difference was noted in wt/*3 heterozygous variant carriers. Conclusion The presence of *2, *4 and *10 alleles was observed to significantly compromise the drug efficacy. *3 allele was found to bear no relation to the effect of diltiazem on achieving rate control.

BackgroundThis study seeks to investigate the distribution of the angiotensin-converting enzyme (ACE) gene polymorphism and serum levels in patients with viral pneumonia and predict which polymorphism will lead to severe progression of the disease. MethodologyThe serum ACE levels and ACE gene polymorphisms were successfully evaluated with respect to subsequent viral pneumonia using records of 100 patients with viral pneumonia and 100 healthy controls. ResultsACE serum concentration was statistically significantly elevated. ACE serum concentration with a cut-off value of ≥5,256.05 pg/mL had 85.3% sensitivity and 83.2% selectivity. In addition, patients with ACE genotype D/D were 0.08 times more likely to manifest severe lung involvement than those with I/I, and patients with the I/D genotype were 0.02 times more likely than their counterparts with I/I. The computed tomography findings of the patients revealed that ACE serum concentration was significantly effective in discriminating between mild and moderate-to-severe lung involvement. No significant difference was observed between the blood parameters and ACE genotype distributions. ConclusionsI/D polymorphism likely affects the expression of the ACE gene and/or the function of the angiotensin I converting enzyme. The D/D genotype is associated with vessel wall thickness and higher blood pressure. Strong evidence was found between D/D and I/D genotypes in the patient cohort concerning genotypes and ACE serum concentration. Further analysis showed that ACE serum levels were more elevated in the D/D genotype compared to the I/D genotype in the patient cohort.

Objective: This study aims to evaluate the relationship between peroxisome proliferator-activated receptor (PPAR) alpha and gamma gene polymorphisms and acute coronary syndrome (ACS) clinically. Subject and methods: Peripheral blood samples were collected from a total of 200 people, including 100 acute coronary syndrome patients and 100 controls aged 19 to 93 years, admitted to the Pamukkale University Emergency Medicine Department. The healthy volunteers had no known chronic or acute diseases, no history of drug use, and no recent history of coronary artery disease (CAD). PPAR alpha L162V and PPAR gamma C161T gene polymorphic regions were detected using DNA sequencing analyses. In addition, data collected from the hemogram and biochemical parameters and comorbidities of the patients were statistically analyzed. Results: PPAR gamma C161T polymorphisms were compared between groups. The CT heterozygous rate in the patient group (74%) was higher than in the control group (7%). The T allele was more common in the patient group (0.37) compared to the control group (0.03). When PPAR alpha L162V polymorphism was compared, VV homozygous individuals were %19 in the patient group and none in the control group. The V allele was found to be statistically higher in patients with ACS (p<0.01). Conclusion: The findings revealed that elevated PPAR alpha L162V and PPAR gamma C161T gene polymorphisms were associated with a progressive risk of ACS.